There is robust support for heritable influences on alcohol use and AUD (twin heritability ~30–40% and 50%, respectively; Koopmans, Slutske, van Baal, & Boomsma, 1999; Verhulst, Neale, & Kendler, 2015; Viken, Kaprio, Koskenvuo, & Rose, 1999), as well as for impulsivity, risk-taking, negative urgency, depression, and EF (Anokhin, Grant, Mulligan, & Heath, 2015; Flint & Kendler, 2014; Friedman et al., 2008; Gustavson et al., 2020), with well-powered genome-wide association studies (GWAS) identifying loci that contribute to this heritable variation (Hatoum et al., 2023; Karlsson Linnér et al., 2019; Levey et al., 2021; Zhou et al., 2020). Incorporating estimates of this genetic liability into theoretical frameworks and analytic models of the relationships between these phenotypes can help clarify the extent to which their association is explained by shared genetic predisposition. Indeed, the Genetically Informed Neurobiological model of Addiction (GINA; Bogdan et al., 2023) posits that genetically influenced individual differences in impulsivity/risk-taking, negative urgency and depression, and EF confer differential vulnerability to the initial seeking and acutely rewarding aspects of substances, heightened negative affect with chronic use, and difficulty engaging in goal-directed behavior when salient substance-related cues elicit craving.
